Elsevier

International Journal of Cardiology

Volume 299, 15 January 2020, Pages 110-115
International Journal of Cardiology

Myocardial blood flow and cardiac sympathetic innervation in young adults late after arterial switch operation for transposition of the great arteries

https://doi.org/10.1016/j.ijcard.2019.07.041Get rights and content

Highlights

  • Cardiac innervation is reduced in young adults after the arterial switch operation.

  • Myocardial blood flow at rest and after adenosine stimulation is limited.

  • Myocardial blood flow response capacity to a sympathetic stimulus is reduced.

Abstract

Background

The arterial switch operation (ASO) for repair of transposition of the great arteries (TGA) requires transection of the great arterial trunks and re-implantation of the coronary arteries into the neoaortic root resulting in cardiac sympathetic denervation which may affect myocardial blood flow (MBF) regulation. The aims of the present study were to evaluate sympathetic (re-)innervation in young adults after ASO and its impact on MBF.

Methods

Twelve patients (age 22.5 ± 2.6 years) after ASO for TGA in the neonatal period and ten healthy controls (age 22.0 ± 1.7 years) were included. Positron emission tomography (PET) was used for measuring cardiac sympathetic innervation with [11C]meta-hydroxyephedrine (mHED) and MBF with [15O]H2O PET at rest, during adenosine stimulation, and during sympathetic stimulation with cold pressor test. Cold pressor-induced MBF response capacity was calculated as maximal global MBF over peak rate-pressure product multiplied by 10′000.

Results

Global [11C]mHED uptake was significantly lower in patients compared to controls (7.0 ± 2.3 versus 11.8 ± 2.1%/min, p < 0.001). Global MBF was lower in patients compared to controls at rest and during adenosine-induced hyperemia (0.66 ± 0.08 versus 0.82 ± 0.15 ml/min/g, p = 0.005; 2.23 ± 1.19 versus 3.36 ± 1.04 ml/min/g, p = 0.030, respectively). Interestingly, MBF during cold pressor test did not differ between patients and controls (0.99 ± 0.20 versus 1.07 ± 0.16 ml/min/g, p = 0.330). However, cold pressor-induced MBF response capacity was significantly lower for patients as compared to controls (1.09 ± 0.35 versus 1.44 ± 0.39 ml/g/10,000 mmHg, p = 0.040).

Conclusions

With only partial sympathetic re-innervation of the coronary arteries, maximal dilator capacity of the coronary microvasculature and cold pressor-induced MBF response capacity remain substantially impaired in young adults after ASO compared to healthy controls.

Introduction

Complete transposition of the great arteries (TGA) is the most common cyanotic congenital heart disease presenting in the newborn period affecting 0.2 per 1000 newborns [1]. Without intervention, its prognosis is grim [2]. The arterial switch operation (ASO), successfully invented by Jatene in 1975 [3], has become the surgical procedure of choice for repair of TGA and has superseded the atrial switch operation [4]. Short and midterm outcomes after the ASO are good, and the cohort of adult survivors after the ASO is rapidly growing [4].

The ASO requires transection of the great arterial trunks with re-implantation of the coronary arteries into the neoaortic root [3]. As cardiac sympathetic fibres travel along the coronary vessels [5], ASO inevitably results in the dissection of the sympathetic fibres and as a consequence in sympathetic denervation of the heart, which may impact the regulation of myocardial blood flow (MBF) as seen in patients after heart transplantation [6,7]. In children after the ASO, previous studies have demonstrated reduced MBF [8] and at least partial sympathetic re-innervation until childhood [9]. However, little is known about the extent of sympathetic re-innervation in young adults after ASO and the impact of sympathetic innervation on MBF.

The aims of the present study were, therefore, to assess cardiac sympathetic innervation in young adults after the ASO and its impact on MBF by positron-emission tomography (PET).

Section snippets

Study population

Fourteen adult patients (>18 years) who had undergone the ASO for d-TGA in the neonatal period were recruited from three adult congenital heart disease centres in Switzerland. Exclusion criteria were allergies against iodine-containing contrast dye, current intake of beta blockers or nitroglycerine, kidney dysfunction with a creatinine clearance of <60 ml/min, ongoing cardiac arrhythmia, high grade AV-block, asthma, chronic obstructive pulmonary disease, pregnancy, breastfeeding, and intake of

Baseline characteristics

Twelve patients and 10 healthy controls were included. The mean age of patients and controls was 22.5 ± 2.6 and 22.0 ± 1.7 years, respectively (p = 0.546). 11 patients (92%) and 9 controls (90%) were male (p = 0.892). Patient characteristics of the study population are depicted in Table 1. Left ventricular ejection fraction was normal in all patients (mean 58.4 ± 3.7%, range 52–65%). Six patients had a smoking history (range 1–6 pack years), none of the healthy controls were smokers. None of

Discussion

The present study is the first to assess MBF and cardiac sympathetic innervation in young adult patients (mean age 22.5 ± 2.6 years) late after ASO for TGA. Our results demonstrate that while partial cardiac sympathetic innervation was present in all patients, global cardiac sympathetic innervation was still significantly lower in patients after ASO compared to their healthy counterparts. Nevertheless, MBF response to a sympathetic stimulus based on a standardised cold pressor test did not

Conclusions

With only partial sympathetic re-innervation of the coronary arteries, maximal dilator capacity of the coronary microvasculature and cold pressor-induced MBF response capacity remain substantially impaired in young adults after ASO compared to healthy controls.

The following is the supplementary data related to this article.

. Circulating catecholamines at rest and during cold pressor test.

Sources of funding

None.

Declaration of Competing Interest

The University Hospital Zurich holds a research agreement with GE Healthcare.

Acknowledgements

None.

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